Microglia serve as the first and main form of active immune defense in the central nervous system. These cells are believed to be functionally equivalent to monocytes or tissue macrophages of the somatic immune system. It has long been recognized that microglia migrate to, differentiate and proliferate at sites of brain injury and inflammation. Thus, activation of microglia appears to play a major role in numerous neuroinflammatory diseases or disorders. Furthermore, microglial activation is modulated by opiates and has been implicated in opiate dependence and the development of tolerance. The mu opiate receptor antagonists, (−)-naloxone and (−)-naltrexone, have been shown to inhibit the proinflammatory pathway involved in microglial activation. Inhibition of microglial activation is non-stereoselective, however, in that the (+) mirror enantiomers of naloxone and naltrexone have been shown to retain microglial inhibitory activity. Thus, (+)-morphinan compounds may be useful for treating inflammatory diseases, as antitussive agents, or for reducing the potential of opiate abuse and dependence. Substitution at position 6 of the morphinan ring may provide compounds that function as prodrugs with increased activity relative to the unfunctionalized precursors. There is a need, therefore, for mirror image enantiomorph (+)-morphinan compounds with substituted hydroxy or amino groups at position 6.